Human papillomaviruses (HPVs) have previously been reported to infect epithelial trophoblast cells of the placenta. influences these infections. hybridization has shown that HPV DNA can be localized in placental trophoblasts [10]. The trophoblast 3A cell line has been reported to support HPV16 and 31 replication though the permissiveness of primary trophoblasts to HPV infection remains unclear [11] [12]. Iloperidone Besides mediating nutrient and gas exchange between the fetus and mother the fetal trophoblast cells are in direct contact with the maternal tissues and play a crucial role in the process of placentation [13]. Based on this intimate contact and communication between the maternal and fetal sides of the placenta it is thought that infection with HPV may result in death of placental trophoblasts or malfunction in recognition of endometrial cells or even malignancy. Changes may consequently disrupt the integrity of the trophoblast layer and cause spontaneous abortions or preterm delivery [13] [14]. Together these studies motivated us to investigate placental HPV particularly in the context of HIV infection. Human papillomavirus (HPV) infections are more Iloperidone abundant in human HIV-positive individuals [15]. HIV-positive women have a high prevalence of HPV-induced dysplasias of the cervix [16]–[18]. Similarly a study conducted by Ahdieh and colleagues showed that HIV-positive women were 1.8 2.1 and 2.7 times more likely to harbor high- intermediate- and low-risk HPV infections respectively than HIV-negative women. The persistence of HPV Iloperidone lesions was approximately two times longer in women with a CD4 cell count less than 200 cells/μl compared to those with greater than 500 cells/μl [19]. The risk for Iloperidone acquisition of HPV is directly related to the number of sexual partners. This is in agreement with other findings that HIV-positive individuals tend to have a higher prevalence of anogenital HPV infections [17] [20] with a lower CD4+ count which is predictive of anogenital intraepithelial neoplasia. The importance of cell-mediated immunity in the control of HPV infection has been evidenced by studies that have documented an increased prevalence and progression of HPV infections in the immunosuppressed [21] [22]. Multiple recurrences of cervical HPV infections occur in HIV infected patients and anti-retroviral drugs do not appear to thoroughly suppress these relapses [22] [23]. HIV attenuates the systemic immune response against HPV via its effect on CD4+ cells and regulation of immune responses to different types of antigens. A low number of circulating HPV specific memory cells is thought to make the HPV-specific immunity defective and promote disease progression [17]. The derepression of high-risk HPV replication by HIV has been reported elsewhere [17] [21] [22]. However there is still relatively little known about the role of HIV in HPV pathogenesis in the placental compartments. In the present study we chose to investigate HPV genotype distributions in the placental compartment as a function of HIV status. We found evidence of 3 HPV genotypes in placenta (type 6 16 and 90) whereas vaginal sampling of the same patient population recovered 20 different HPV genotypes [24]. In our Mouse monoclonal antibody to Keratin 7. The protein encoded by this gene is a member of the keratin gene family. The type IIcytokeratins consist of basic or neutral proteins which are arranged in pairs of heterotypic keratinchains coexpressed during differentiation of simple and stratified epithelial tissues. This type IIcytokeratin is specifically expressed in the simple epithelia lining the cavities of the internalorgans and in the gland ducts and blood vessels. The genes encoding the type II cytokeratinsare clustered in a region of chromosome 12q12-q13. Alternative splicing may result in severaltranscript variants; however, not all variants have been fully described. previous study we found that HIV Iloperidone infection was associated with higher incidence of HPV18 in the vaginal compartment. In the present study we find that HIV-positive patients are about 2-fold more likely to test positive for HPV16 in the placental compartment then those who are HIV-negative supporting the concept that HPV infections placenta is evidence of HPV16 L1 major capsid protein expression in placental samples from either HIV positive or negative women. Furthermore we performed hybridization which showed the presence of HPV16 DNA in placental trophoblast cells. 2 Materials and Methods Study Participants Between March 1998 and October 2004 3161 pregnant women who were admitted to the labor ward at the University Teaching Hospital (UTH) in Lusaka Zambia were recruited for a cohort study to investigate HIV infection. This study was under institutional IRB approval at the University of Nebraska-Lincoln and the University of Zambia. Women were enrolled into the study with written consent. Placentas from 213 women were selected randomly collected for further study. 2.1 Sample Collection All tissues were obtained under consent from HIV-negative Iloperidone and.